Amprion wins $100K to study causes of sporadic ALS
Study found that 15% of sporadic ALS patients had misfolded alpha-synuclein
Amprion has been awarded a $100,000 research grant to support studies on the causes of sporadic amyotrophic lateral sclerosis (ALS) that could help diagnose and develop potential therapies for the disease.
The project, led by Richard Smith, MD, state director of the Center for Neurologic Study, and Amprion’s co-founder Russ Liebovitz, MD, PhD, was funded through the ALS Network‘s global research program. It will explore how clumps of misfolded alpha-synuclein protein, a hallmark of Parkinson’s that’s found in about 15% of sporadic ALS patients, contribute to ALS disease progression and symptoms. Researchers at Amprion will also work to develop new tests to detect other proteins that are abnormally folded in ALS, which may aid in accelerating the disease’s diagnosis.
“Dr. Smith and the Amprion team have already unearthed a subgroup of ALS patients in which misfolded alpha-synuclein is detected and likely contributes to disease symptoms and possibly progression, ” Lebovitz said in a company press release.
ALS is caused by the progressive damage and death of motor neurons, the specialized nerve cells that control muscle movements. Several mechanisms have been associated with the disease’s progression, including the production of abnormal proteins that accumulate and form toxic clumps in neurons.
Alpha-synuclein and sporadic ALS
Some of the key proteins known to aggregate in ALS include TDP-43, SOD1, and FUS. Smith and Lebovitz showed alpha-synuclein also forms aggregates in some people with ALS.
Researchers discovered this with Amprion’s seed amplification assay (SAA), which uses a sample of cerebrospinal fluid (CSF), the fluid that surrounds the brain and spinal cord, to detect the presence of the abnormal alpha-synuclein.
The funding will help determine if people with abnormal alpha-synuclein or other misfolded proteins have distinct disease characteristics than those who lack those misfolded proteins.
“The ALS Network’s grant will fund additional work as we seek to correlate the contribution of [alpha-synuclein] to clinical features such as rapid progression, Parkinson’s symptoms, sleep disorders, or cognitive decline,” Lebovitz said.
A study that confirms the association “would be a compelling basis for developing a treatment strategy for this variant of ALS,” Smith said.
The ALS Network research program is intended to support projects that seek to identify ALS prevention strategies, develop new treatments, and find a cure for the disease. The organization’s scientific advisory committee is composed of world-renowned researchers, scientists, and healthcare industry leaders who review and select the most promising projects for funding.
“We seek to move promising science forward quickly with a relentless focus on improving and saving lives. Amprion’s work will help accelerate the discovery of therapies for ALS and other motor neuron diseases,” Sheri Strahl, president and CEO of the ALS Network, said.
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